Heart failure affects approximately 5 million people in the United States. Many moderate to severe heart failure patients may also have a condition in which the two lower chambers of the heart (known as the left and right ventricles) are not beating together as they do normally. In medical terms, this condition is called “ventricular dysynchrony.” Ventricular dysynchrony disturbs the synchronous beating of the heart, and as a result the heart does not adequately pump blood to meet the needs of the body. More specifically, ventricular dysynchrony typically results from intraventricular conduction delays iii(IVCD) that disturb the synchronous beating of the ventricles. Typically, the IVCD has a left bundle branch block (LBBB) morphology.
One therapy to treat left ventricle dysynchrony is cardiac resynchronization therapy (CRT), which, when used in combination with stable, optimal medical therapy, is designed to reduce symptoms by restoring the sequence of electrical and mechanical ventricular activation. Cardiac resynchronization therapy (CRT) provides atrial-synchronized, biventricular pacing using standard pacing technology combined with a special third lead implanted via the coronary sinus and positioned in a cardiac vein to sense and pace the left ventricle. Following a sensed atrial contraction, both ventricles are stimulated to contract more synchronously. The resulting resynchronization of ventricular contraction reduces mitral regurgitation and optimizes left ventricular filling and ejection, thereby improving cardiac function.
Currently available CRT bi-ventricular pacing generally employs one lead positioned in operative communication with the right ventricle (RV) and one lead in operative communication with a portion of one of the tributaries of the coronary venous system. The myocardial venous system provides a pathway for deployment of a left ventricular stimulation lead (and associated electrodes) to operatively communicate with the left ventricle. In most patients, an additional lead is deployed to the right atrium (RA) for atrioventricular (AV) synchronization during pacing. Exceptions for placement of the atrial lead include patients suffering from chronic atrial fibrillation (AF) or having a relatively high AF “burden.” According to such CRT delivery, electrical stimulation of both the right and left ventricle operates to assist ventricular asynchrony and increase contractility, as measured by ventricular pressure development (dP/dt). For certain patients, further assistance of contractility can be achieved by variation of the inter-ventricular interval.
The timing between atrial and ventricular pacing is determined by the programmed value of the atrio-ventricular (AV) delay. The timing between right- and left-ventricular pacing pulses is determined by the programmed value of the inter-ventricular (VV) delay. Several acute studies have demonstrated a significant correlation of cardiac function to programmed values of atrioventricular (AV) and interventicular (VV) delays. While AV delay optimization is primarily focused on ensuring synchrony of the atrial and ventricular contractions, the goal of VV delay optimization is to decrease intraventricular mechanical dyssynchrony. Since there is a link between electrical and mechanical activation of the left ventricle during biventricular pacing, decreasing electrical dyssynchrony typically improves left ventricular mechanical function. In order to achieve the greatest improvement in left ventricular contractility, it is desirable to determine an interventricular time delay that corresponds to the maximal electrical synchrony of the left ventricle, known as the optimal VV delay.
When both the left and right ventricular pacing pulses contribute to left ventricular activation, electrical fusion of the two paced wavefronts occurs. The range of VV delays where fusion of the two paced wavefronts can be observed is termed the biventricular pacing window (also called the fusion band). This range may vary from patient to patient and may also be dependent on lead location, conduction disorder, and scar location.
Current methods for determining VV optimization require the use of echocardiography to evaluate the filling, cardiac output, and degree of ventricular dyssynchrony that occurs for different VV settings. Unfortunately, determinations of optimal VV delay settings using echocardiography are time consuming and typically require a burdensome amount of clinical resources. Therefore, what is needed is an improved method and apparatus for determining an optimal VV delay necessary to efficiently and chronically deliver and control a pacing therapy to effect ventricular fusion associated with bi-ventricular CRT pacing therapy.